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Revista Espanola de Cardiologia... Apr 2022
Topics: Cardiomegaly; Humans; Hypertension; Hypertrophy, Left Ventricular
PubMed: 34953764
DOI: 10.1016/j.rec.2021.10.017 -
Calcified Tissue International Mar 2015In a mature (weight neutral) animal, an increase in muscle mass only occurs when the muscle is loaded sufficiently to cause an increase in myofibrillar protein balance.... (Review)
Review
In a mature (weight neutral) animal, an increase in muscle mass only occurs when the muscle is loaded sufficiently to cause an increase in myofibrillar protein balance. A tight relationship between muscle hypertrophy, acute increases in protein balance, and the activity of the mechanistic target of rapamycin complex 1 (mTORC1) was demonstrated 15 years ago. Since then, our understanding of the signals that regulate load-induced hypertrophy has evolved considerably. For example, we now know that mechanical load activates mTORC1 in the same way as growth factors, by moving TSC2 (a primary inhibitor of mTORC1) away from its target (the mTORC activator) Rheb. However, the kinase that phosphorylates and moves TSC2 is different in the two processes. Similarly, we have learned that a distinct pathway exists whereby amino acids activate mTORC1 by moving it to Rheb. While mTORC1 remains at the forefront of load-induced hypertrophy, the importance of other pathways that regulate muscle mass are becoming clearer. Myostatin, is best known for its control of developmental muscle size. However, new mechanisms to explain how loading regulates this process are suggesting that it could play an important role in hypertrophic muscle growth as well. Last, new mechanisms are highlighted for how β2 receptor agonists could be involved in load-induced muscle growth and why these agents are being developed as non-exercise-based therapies for muscle atrophy. Overall, the results highlight how studying the mechanism of load-induced skeletal muscle mass is leading the development of pharmaceutical interventions to promote muscle growth in those unwilling or unable to perform resistance exercise.
Topics: Animals; Humans; Hypertrophy; Muscle, Skeletal; Resistance Training
PubMed: 25359125
DOI: 10.1007/s00223-014-9925-9 -
American Journal of Orthodontics and... Jul 2023Rapid maxillary expansion (RME) expands the maxillary dentition laterally and improves nasal airway obstruction. However, the incidence of nasal airway obstruction...
INTRODUCTION
Rapid maxillary expansion (RME) expands the maxillary dentition laterally and improves nasal airway obstruction. However, the incidence of nasal airway obstruction improvement after RME is approximately 60%. This study aimed to clarify the beneficial effects of RME on nasal airway obstruction in specific pathologic nasal airway diseases (nasal mucosa hypertrophy and obstructive adenoids) using computer fluid dynamics.
METHODS
Sixty subjects (21 boys; mean age 9.1 years) were divided into 3 groups according to their nasal airway condition (control, nasal mucosa hypertrophy, and obstructive adenoids), and those requiring RME had cone-beam computed tomography images taken before and after RME. These data were used to evaluate the nasal airway ventilation condition (pressure) using computer fluid dynamics and measure the cross-sectional area of the nasal airway.
RESULTS
The cross-sectional area of the nasal airway significantly increased after RME in all 3 groups. The pressures in the control and nasal mucosa groups significantly reduced after RME but did not change significantly in the adenoid group. The incidence of improvement in nasal airway obstruction in the control, nasal mucosa, and adenoid groups was 90.0%, 31.6%, and 23.1%, respectively.
CONCLUSIONS
The incidence of improvement in nasal airway obstruction after RME depends on the nasal airway condition (nasal mucosa hypertrophy and obstructive adenoids). In patients with nonpathologic nasal airway conditions, the obstruction may be sufficiently improved with RME. Furthermore, to some extent, RME may be effective in treating nasal mucosa hypertrophy. However, because of obstructive adenoids, RME was ineffective in patients with nasal airway obstruction.
Topics: Male; Humans; Child; Nasal Obstruction; Adenoids; Palatal Expansion Technique; Hydrodynamics; Nasal Mucosa; Cone-Beam Computed Tomography; Hypertrophy
PubMed: 37191595
DOI: 10.1016/j.ajodo.2023.04.014 -
World Journal of Urology Nov 2023To identify expert laser settings for BPH treatment and evaluate the application of preventive measures to reduce complications.
Experts' recommendations in laser use for the endoscopic treatment of prostate hypertrophy: a comprehensive guide by the European Section of Uro-Technology (ESUT) and Training-Research in Urological Surgery and Technology (T.R.U.S.T.)-Group.
PURPOSE
To identify expert laser settings for BPH treatment and evaluate the application of preventive measures to reduce complications.
METHODS
A survey was conducted after narrative literature research to identify relevant questions regarding laser use for BPH treatment (59 questions). Experts were asked for laser settings during specific clinical scenarios. Settings were compared for the reported laser types, and common settings and preventive measures were identified.
RESULTS
Twenty-two experts completed the survey with a mean filling time of 12.9 min. Ho:YAG, Thulium fiber laser (TFL), continuous wave (cw) Tm:YAG, pulsed Tm:YAG and Greenlight™ lasers are used by 73% (16/22), 50% (11/22), 23% (5/22), 13.6% (3/22) and 9.1% (2/22) of experts, respectively. All experts use anatomical enucleation of the prostate (EEP), preferentially in one- or two-lobe technique. Laser settings differ significantly between laser types, with median laser power for apical/main gland EEP of 75/94 W, 60/60 W, 100/100 W, 100/100 W, and 80/80 W for Ho:YAG, TFL, cwTm:YAG, pulsed Tm:YAG and Greenlight™ lasers, respectively (p = 0.02 and p = 0.005). However, power settings within the same laser source are similar. Pulse shapes for main gland EEP significantly differ between lasers with long and pulse shape modified (e.g., Moses, Virtual Basket) modes preferred for Ho:YAG and short pulse modes for TFL (p = 0.031).
CONCLUSION
Ho:YAG lasers no longer seem to be the mainstay of EEP. TFL lasers are generally used in pulsed mode though clinical applicability for quasi-continuous settings has recently been demonstrated. One and two-lobe techniques are beneficial regarding operative time and are used by most experts.
Topics: Male; Humans; Lithotripsy, Laser; Prostatic Hyperplasia; Prostate; Lasers, Solid-State; Hypertrophy; Thulium; Laser Therapy
PubMed: 37632557
DOI: 10.1007/s00345-023-04565-y -
Circulation. Cardiovascular Imaging Oct 2023Severe aortic stenosis (AS) is associated with left ventricular (LV) hypertrophy and cardiac metabolic alterations with evidence of steatosis and impaired myocardial...
BACKGROUND
Severe aortic stenosis (AS) is associated with left ventricular (LV) hypertrophy and cardiac metabolic alterations with evidence of steatosis and impaired myocardial energetics. Despite this common phenotype, there is an unexplained and wide individual heterogeneity in the degree of hypertrophy and progression to myocardial fibrosis and heart failure. We sought to determine whether the cardiac metabolic state may underpin this variability.
METHODS
We recruited 74 asymptomatic participants with AS and 13 healthy volunteers. Cardiac energetics were measured using phosphorus spectroscopy to define the myocardial phosphocreatine to adenosine triphosphate ratio. Myocardial lipid content was determined using proton spectroscopy. Cardiac function was assessed by cardiovascular magnetic resonance cine imaging.
RESULTS
Phosphocreatine/adenosine triphosphate was reduced early and significantly across the LV wall thickness quartiles (Q2, 1.50 [1.21-1.71] versus Q1, 1.64 [1.53-1.94]) with a progressive decline with increasing disease severity (Q4, 1.48 [1.18-1.70]; =0.02). Myocardial triglyceride content levels were overall higher in all the quartiles with a significant increase seen across the AV pressure gradient quartiles (Q2, 1.36 [0.86-1.98] versus Q1, 1.03 [0.81-1.56]; =0.034). While all AS groups had evidence of subclinical LV dysfunction with impaired strain parameters, impaired systolic longitudinal strain was related to the degree of energetic impairment (=0.219; 0.03). Phosphocreatine/adenosine triphosphate was not only an independent predictor of LV wall thickness (=-0.20; =0.04) but also strongly associated with myocardial fibrosis (=-0.24; =0.03), suggesting that metabolic changes play a role in disease progression. The metabolic and functional parameters showed comparable results when graded by clinical severity of AS.
CONCLUSIONS
A gradient of myocardial energetic deficit and steatosis exists across the spectrum of hypertrophied AS hearts, and these metabolic changes precede irreversible LV remodeling and subclinical dysfunction. As such, cardiac metabolism may play an important and potentially causal role in disease progression.
Topics: Humans; Phosphocreatine; Hypertrophy, Left Ventricular; Aortic Valve Stenosis; Adenosine Triphosphate; Cardiomyopathies; Fibrosis; Phenotype; Disease Progression; Ventricular Function, Left
PubMed: 37847766
DOI: 10.1161/CIRCIMAGING.122.014863 -
Urology Jul 2019To evaluate the incidence and durability of compensatory hypertrophy with solitary kidneys in the setting of those with multicystic dysplastic kidney (MCDK) or Wilms...
OBJECTIVE
To evaluate the incidence and durability of compensatory hypertrophy with solitary kidneys in the setting of those with multicystic dysplastic kidney (MCDK) or Wilms tumor (WT) status postnephrectomy.
PATIENTS AND METHODS
We conducted a retrospective cohort study of patients with MCDK and WT. MCDK patients were verified by sonographic findings prenatally. WT patients entered our study at time of nephrectomy. We compared the natural history of hypertrophy between the 2 cohorts via renal length measurement. We performed linear regression to predict creatinine clearance from renal length after adjusting for age and cohort status (MCDK versus WT).
RESULTS
Fifty-two patients (56%) were diagnosed with WT, and 71 patients (44%) with MCDK patients met study criteria with a median age of postnatal ultrasound at 1.6 months (interquartile range 0.5-3.6). The median (IQR) follow-up time was 7.5 years. At the time of nephrectomy, 25/52 (48%) of Wilms patients had contralateral hypertrophy, while at diagnosis 22/71 (31%) of MCDK patients had contralateral hypertrophy, P = .03. Contralateral hypertrophy was a consistent finding throughout follow-up. As renal length increases by 1 cm, glomerular filtration rate increased by 7.8 mL/min/m (95% confidence interval 1.8-13.8, P = .01).
CONCLUSION
Contralateral hypertrophy appears to be a compensatory mechanism for unilateral kidney pathology as demonstrated by MCDK and WT patients. Hypertrophy often occurs at the time of diagnosis and appears to be a permanent finding as children reach their teenage years. Additionally, in nonhydronephrotic kidneys, increases in renal length correlate with improvement in glomerular filtration rate. Overall, the majority of children with solitary kidneys demonstrate compensatory hypertrophy.
Topics: California; Child, Preschool; Female; Follow-Up Studies; Forecasting; Humans; Hypertrophy; Incidence; Infant; Infant, Newborn; Kidney; Male; Nephrectomy; Postoperative Period; Retrospective Studies; Solitary Kidney
PubMed: 30986483
DOI: 10.1016/j.urology.2019.04.003 -
International Journal of Molecular... Apr 2022Long noncoding RNA (lncRNA) plays a crucial part in all kinds of life activities, especially in myogenesis. (SWI/SNF-related, matrix-associated, actin-dependent...
Long noncoding RNA (lncRNA) plays a crucial part in all kinds of life activities, especially in myogenesis. (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily d, member 3) is a member of the SWI/SNF protein complex and was reported to be required for cell proliferation and myoblast differentiation. In this study, we identified a new lncRNA named (), which strongly regulated the development of myogenesis by improving the expression of (). We overexpressed and knockdown the expression of and to investigate their function on myoblast proliferation and differentiation. Cell experiments proved that and promoted myoblast proliferation through the pathway and improved differentiation of differentiated myoblasts through the pathway. Moreover, they upregulated the fast-twitch fiber-related genes and downregulated the slow-twitch fiber-related genes, which indicated that they facilitated the slow-twitch fiber to transform into the fast-twitch fiber. The animals' experiments supported the results above, demonstrating that could induce muscle hypertrophy and fast-twitch fiber transformation. In conclusion, can improve the expression of , thus inducing muscle hypertrophy. In addition, can facilitate slow-twitch fibers to transform into fast-twitch fibers.
Topics: Animals; Cell Differentiation; Hypertrophy; Muscle Development; Muscles; Myoblasts; RNA, Long Noncoding
PubMed: 35562902
DOI: 10.3390/ijms23094510 -
Cancer Research May 2022Heart failure and cancer are the leading cause of deaths worldwide. While heart failure and cancer have been considered separate diseases, it is becoming evident that...
UNLABELLED
Heart failure and cancer are the leading cause of deaths worldwide. While heart failure and cancer have been considered separate diseases, it is becoming evident that they are highly connected and affect each other's outcomes. Recent studies using experimental mouse models have suggested that heart failure promotes tumor progression. The mouse models used involve major irreversible surgery. Here, we induced heart hypertrophy via expression of activating transcription factor 3 (ATF3) in cardiomyocytes, followed by cancer cells' implantation. Tumors developing in ATF3-transgenic mice grew larger and displayed a more highly metastatic phenotype compared with tumors in wild-type mice. To address whether ATF3 expression or the cardiac outcome are necessary for tumor progression, ATF3 expression was turned off after cardiac hypertrophy development followed by cancer cell implantation. The tumor promotion phenotype and the enhancement of metastatic properties were preserved, suggesting that the failing heart per se is sufficient to promote tumor progression. Serum derived from ATF3-transgenic mice enhanced cancer cell proliferation and increased cancer cell metastatic properties in vitro. Using a cytokine array panel, multiple factors responsible for promoting tumor cell proliferation and the metastatic phenotype were identified. Interestingly, the failing heart and the tumor separately and simultaneously contributed to higher levels of these factors in the serum as well as other tissues and organs. These data suggest the existence of intimate cross-talk between the hypertrophied heart and the tumor that is mediated by secreted factors, leading to cancer promotion and disease deterioration.
SIGNIFICANCE
This work highlights the importance of early diagnosis and treatment of heart failure prior to reaching the irreversible stage that can exacerbate cancer progression.
Topics: Activating Transcription Factor 3; Animals; Cardiomegaly; Heart Failure; Humans; Mice; Mice, Inbred C57BL; Mice, Transgenic; Neoplasms; Ventricular Remodeling
PubMed: 35260887
DOI: 10.1158/0008-5472.CAN-21-2463 -
The Spine Journal : Official Journal of... Jun 2021Ligamentum flavum (LF) hypertrophy plays a dominant role in lumbar spinal stenosis (LSS). A previous study found that fibroblast growth factor 9 (FGF9) was upregulated...
BACKGROUND CONTEXT
Ligamentum flavum (LF) hypertrophy plays a dominant role in lumbar spinal stenosis (LSS). A previous study found that fibroblast growth factor 9 (FGF9) was upregulated with mechanical stress in rabbit LF. However, the expression and function of FGF9 are not well understood in human LF.
PURPOSE
To evaluate FGF9 expression and function in human LF with and without hypertrophy.
STUDY DESIGN
This study employed a basic research study design utilizing human LF tissue for histological analyses.
PATIENT SAMPLES
Hypertrophied LF tissue sample from patients with LSS, and nonhypertrophied (control) LFs from patients with lumbar disc herniation or other diseases were obtained during surgery.
METHODS
LF specimens were histologically analyzed for FGF9 and vascular endothelial growth factor A (VEGF-A) by immunohistochemistry. The number of total and FGF9 immuno-positive cells and blood vessels were counted and compared between LF with and without hypertrophy. For functional analysis, the effect of FGF9 on cell proliferation and migration was examined using a primary cell culture of human LF.
RESULTS
Histological studies revealed that the total cell number was significantly higher in the LF of patients with LSS than in the LF of control patients. Immunohistochemistry showed that the percentage of FGF9-positive cells was significantly higher in the LF of patients with LSS than in the controls, and it positively correlated with patients' age, regardless of disease. Double immune-positive cells for FGF9 and VEGF-A were often observed in vascular endothelial cells and fibroblasts in the fibrotic area of hypertrophied LF, and the number of double positive vessels was significantly higher in LF of LSS patients than in the LF of controls. Primary cell culture of human LF revealed that FGF9 promoted the proliferation and migration of LF cells.
CONCLUSION
The present study demonstrated that FGF9 expression is highly upregulated in hypertrophied human LF. FGF9 potentially plays a pivotal role in the process of hypertrophy of LF, which is associated with mechanical stress, through cell proliferation and migration.
CLINICAL SIGNIFICANCE
The results from this study partially reveal the molecular mechanisms of LF hypertrophy and suggest that FGF9 may be involved in the process of LF degeneration in elderly patients.
Topics: Aged; Animals; Endothelial Cells; Fibroblast Growth Factor 9; Humans; Hypertrophy; Ligamentum Flavum; Lumbar Vertebrae; Rabbits; Spinal Stenosis; Vascular Endothelial Growth Factor A
PubMed: 33577925
DOI: 10.1016/j.spinee.2021.02.004 -
Scientific Reports Feb 2022Lobar selective internal radiation therapy (SIRT) is widely used to treat liver tumors inducing atrophy of the treated lobe and contralateral hypertrophy. The lack of...
Lobar selective internal radiation therapy (SIRT) is widely used to treat liver tumors inducing atrophy of the treated lobe and contralateral hypertrophy. The lack of animal model has precluded further investigations to improve this treatment. We developed an animal model of liver damage and atrophy-hypertrophy complex after SIRT. Three groups of 5-8 rabbits received transportal SIRT with Yttrium 90 resin microspheres of the cranial lobes with different activities (0.3, 0.6 and 1.2 GBq), corresponding to predicted absorbed radiation dose of 200, 400 and 800 Gy, respectively. Another group received non-loaded microspheres (sham group). Cranial and caudal lobes volumes were assessed using CT volumetry before, 15 and 30 days after SIRT. Liver biochemistry, histopathology and gene expression were evaluated. Four untreated rabbits were used as controls for gene expression studies. All animals receiving 1.2 GBq were euthanized due to clinical deterioration. Cranial SIRT with 0.6 GBq induced caudal lobe hypertrophy after 15 days (median increase 34% -ns-) but produced significant toxicity. Cranial SIRT with 0.3 GBq induced caudal lobe hypertrophy after 30 days (median increase 82%, p = 0.04). No volumetric changes were detected in sham group. Transient increase in serum transaminases was detected in all treated groups returning to normal values at 15 days. There was dose-dependent liver dysfunction with bilirubin elevation and albumin decrease. Histologically, 1.2 GBq group developed permanent severe liver damage with massive necrosis, 0.6 and 0.3 GBq groups developed moderate damage with inflammation and portal fibrosis at 15 days, partially recovering at 30 days. There was no difference in the expression of hepatocyte function and differentiation genes between 0.3 GBq and control groups. Cranial SIRT with 0.3 GBq of Y resin microspheres in rabbits is a reliable animal model to analyse the atrophy-hypertrophy complex and liver damage without toxicity.
Topics: Animals; Atrophy; Female; Hypertrophy; Liver; Liver Diseases; Rabbits; Yttrium Radioisotopes
PubMed: 35110610
DOI: 10.1038/s41598-022-05672-3